Basic physiology of the drainage of aqueous humor

Abstract

The drainage of aqueous humor is discussed on the basis of previously reported results and results included in this communication. Water, solutes and small particulate material such as cell fragments are drained from the anterior chamber with a bulk flow of aqueous humor into the iridocorneal angle. In primates most of the fluid passes through the uveal, corneo-scleral and endothelial meshwork into the canal of Schlemm to be drained through collector channels into intrascleral, episcleral and conjunctival veins. There is also a drainage of fluid through the interstitial tissue spaces of the ciliary muscle into the supraciliary and supra-choroidal spaces. From these spaces fluid may pass through the sclera via spaces between the collagen fibrils in the sclera and through loose connective tissue along nerves and blood vessels piercing the sclera. Exchange by ultrafiltration, diffusion and active transport between the anterior chamber fluid and the surrounding tissues modifies the composition of the anterior chamber fluid but causes practically no net movement of fluid. The structures between the anterior chamber and Schlemm's canal may be regarded as a self-cleaning filter. These structures and the inner wall of Schlemm's canal also have rectifying properties restricting retrograde flow under conditions of a reversal of the normal pressure gradient. The flow from the anterior chamber into Schlemm's canal is pressure dependent. Artificial increments in intraocular pressure (IOP) also affect the routes: opening of more transcellular routes in the inner wall of Schlemm's canal and washout of ground substance tend to reduce the outflow resistance. Moderate increments in IOP have practically no effect on uveoseleral flow. The uveal meshwork is an anterior extension of the connective tissue of the ciliary muscle. Contraction of the muscle causes a rearrangement of the filtering tissue in such a way that the resistance to outflow via Schlemm's canal is reduced. At the same time uveoscleral flow is almost stopped due to compression of the interstitial spaces within the muscle. Experiments with cytochalasin B, epinephrine and EDTA indicate that agents not likely to cause contraction of the ciliary muscle may also cause marked effects on the outflow resistance.